The lymphatic system functions as the primary mechanism by which organs remove excess interstitial fluid and thus prevent accumulation of edema within the interstitial matrix. Recent findings indicate that myocardial edema may be responsible for a myriad of pathologies including diastolic heart failure and the increased pathogenicity of myocardial infarctions in hypertensive patients. We postulated that myocardial edema may compromise cardiac function directly by increasing the disposition of fibrous collagen within the myocardial interstitial matrix or cytoskeleton. Several factors will be studies which directly influence the accumulation of myocardial edema. Studies shall be carried out to evaluate ow changes in myocardial microvascular permeability, microvascular pressures and compromised cardiac lymph flow affect myocardial edema formation. The quantitative affects of edema on cardiac function shall then be documented. Changes within the myocardial interstitial matrix brought on by the presence of edema fluid shall also be documented and their affects on cardiac function quantitated. The edema induced changes to be studies shall include myocardial interstitial compliance (myocardial matrix glycosaminoglycan concentration as well as typing and quantitating of fibrous collagen deposition. New models have also been developed to differentiate the effects myocardial hypertrophy from those of myocardial edema. All studies shall be performed on both normotensive and chronically hypertensive subjects to determine whether myocardial edema and interstitial fibrosis may be in fact be the causative agents in the increased pathogenicity of myocardial infarctions in chronic arterial hypertension. We believe our preliminary findings are unique and exciting and that resolution of the relationship between myocardial lymph flow, myocardial edema and cardiac function could shed significant new light on several clinically important questions which thus far remain unresolved.